Glucocorticoids stimulate ENaC upregulation in bovine mammary epithelium.

Glucocorticoids stimulate ENaC upregulation in bovine mammary epithelium. Research Abstract Details 

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Glucocorticoids stimulate ENaC upregulation in bovine mammary epithelium. Abstract Text:

Rebecca R Quesnell,Xiaobin Han,Bruce D Schultz,

Mammary epithelia produce an isotonic, low-Na(+) fluid that is rich in nutrients. Mechanisms that account for the low electrolyte concentration have not been elucidated, although amiloride-sensitive ion transport has been reported in some situations. We hypothesized that corticosteroid exposure modulates epithelial Na(+) channel (ENaC) expression and/or activity in bovine mammary epithelial cells. BME-UV cells were grown to confluent monolayers on permeable supports with a standard basolateral medium and apical medium of low-electrolyte, high-lactose composition that resembles the ionic composition of milk. Ion transport was assessed in modified Ussing flux chambers. Exposure to glucocorticoids (dexamethasone, cortisol, or prednisolone), but not aldosterone, increased short-circuit current (I(sc)), a sensitive measure of net ion transport, whereas apical exposure to amiloride or benzamil reduced corticosteroid-induced I(sc) close to basal levels. Quantitative RT-PCR indicated a glucocorticoid-induced increase in mRNA for beta- and gamma-ENaC, whereas alpha-ENaC mRNA expression was only mildly affected. Exposure to mifepristone (a glucocorticoid receptor antagonist), but not spironolactone (a mineralocorticoid receptor antagonist), precluded both the corticosteroid-induced elevation in amiloride-sensitive I(sc) and the induced changes in beta- and gamma-ENaC mRNA. We conclude that Na(+) movement across mammary epithelia is modulated by corticosteroids via a glucocorticoid receptor-mediated mechanism that regulates the expression of the beta- and gamma-subunits of ENaC. ENaC expression and activity could account for the low Na(+) concentration that is typical of milk.

Glucocorticoids stimulate ENaC upregulation in bovine mammary epithelium. Publishing Authors By Initials

RR Quesnell,X Han,BD Schultz,

For similar genetic processes: gene expression regulation: up-regulation research abstracts see: genetic processes: gene expression regulation: up-regulation research

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Glucocorticoids stimulate ENaC upregulation in bovine mammary epithelium. Journal Published:

PUBLICATION TYPE: Research Support, U.S. Gov't,

Journal: American journal of physiology. Cell physiology

VOLUME: 292

Page Numbers: C1739-45

Journal Abbreviation: Am. J. Physiol., Cell Physiol.

ISSN: 0363-6143

DAY: 24

MONTH: 01

YEAR: 2007

Glucocorticoids stimulate ENaC upregulation in bovine mammary epithelium. Information

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LANGUAGE: eng

NlmUniqueID: 100901225

Glucocorticoids stimulate ENaC upregulation in bovine mammary epithelium. Keywords Mesh Terms:

KEYWORDS: Up-Regulation

MESH TERMS: pharmacology

Chemical & Substance for Abstract: Glucocorticoids stimulate ENaC upregulation in bovine mammary epithelium. Information

Substance Name: Mifepristone

Registry Number: 84371-65-3

Grant and Affiliation Information for Glucocorticoids stimulate ENaC upregulation in bovine mammary epithelium.

AFFILIATION: Department of Anatomy and Physiology, 228 Coles Hall, Kansas State University, Manhattan, KS 66506, USA.

Country: United States

AGENCY: United States PHS

GRANT: P20-PRO-17686

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MEDLINETA: Am J Physiol Cell Physiol

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